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J Appl Physiol. 2001 Feb;90(2):441-6.
Detrimental effects of complement activation in hemorrhagic shock.
Younger JG, Sasaki N, Waite MD, Murray HN, Saleh EF, Ravage ZA, Hirschl RB, Ward PA, Till GO.
Department of Emergency Medicine, University of Michigan, Ann Arbor, Michigan 48109-0303, USA. jyoungemich.edu
The complement system has been implicated in early inflammatory events and a variety of shock states. In rats, we measured complement activation after hemorrhage and examined the hemodynamic and metabolic effects of complement depletion before injury and worsening of complement activation after hemorrhage and resuscitation [with a carboxypeptidase N inhibitor (CPNI), which blocks the clearance of C5a]. Rats were bled to a mean arterial pressure of 30 mmHg for 50 min and were then resuscitated for 2 h. Shock resulted in significant evidence of complement consumption, with serum hemolytic activity being reduced by 33% (P < 0.05). Complement depletion before injury did not affect hemorrhage volume (complement depleted = 28 +/- 1 ml/kg, complement intact = 29 +/- 1 ml/kg, P = 0.74) but improved postresuscitation mean arterial pressure by 37 mmHg (P < 0.05) and serum bicarbonate levels (complement depleted = 22 +/- 3 meq/ml, complement intact = 13 +/- 8 meq/ml, P < 0.05). Pretreatment with CPNI was lethal in 80% of treated animals vs. the untreated hemorrhaged group in which no deaths occurred (P < 0.05). In this model of hemorrhagic shock, complement activation appeared to contribute to progressive hypotension and metabolic acidosis seen after resuscitation. The lethality of CPNI during acute blood loss suggests that the anaphylatoxins are important in the pathophysiological events involved in hemorrhagic shock.
Online source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11160040&dopt=Abstract hemorrhage
J Pharmacol Exp Ther. 2001 Feb;296(2):284-92.
Trimellitic anhydride-induced allergic response in the guinea pig lung involves antibody-dependent and -independent complement system activation.
Larsen CP, Regal RR, Regal JF.
Department of Pharmacology/Toxicology Graduate Program, University of Minnesota, Duluth, Minnesota 55812-2487, USA.
Trimellitic anhydride (TMA) is one of many low molecular weight compounds known to cause occupational asthma. In our previous studies the TMA-induced allergic response in guinea pigs was attenuated by depletion of complement. Specifically, the leakage of red blood cells and infiltration of inflammatory cells into the lung after TMA challenge was significantly reduced. Thus, we hypothesize that in the presence of specific antibody, TMA activates the complement system and complement activation products play a role in mediating inflammatory cell infiltration into the lung and lung hemorrhage. Guinea pigs were sensitized by intradermal injection of TMA in corn oil. An increase in the complement activation product C3a was detected in bronchoalveolar lavage, but not in plasma, of both sensitized and nonsensitized guinea pigs after intratracheal challenge with TMA conjugated to GPSA (TMA-GPSA). In vitro experiments demonstrated that TMA-GPSA caused complement activation by antibody-dependent as well as antibody-independent pathways. In sensitized animals, TMA-GPSA challenge caused significant increases in eosinophils, neutrophils, and macrophages in lung, along with increases in red blood cells and protein in the airspace. The infiltration of eosinophils was unique in that the magnitude of the GPSA/TMA-GPSA effect was significantly different between nonsensitized and sensitized animals. C3a concentrations in BAL correlated with all measures of cell infiltration in sensitized animals, but not in nonsensitized animals. These data indicate that complement activation in the absence of antibody is not sufficient for the complete allergic response to occur. Both sensitization and the complement system are required for TMA-induced eosinophilia.
Online source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11160609&dopt=Abstract hemorrhage
Neurology. 2001 Jan 23;56(2):190-3.
Circadian and seasonal occurrence of subarachnoid and intracerebral hemorrhage.
Nyquist PA, Brown RD Jr, Wiebers DO, Crowson CS, O'Fallon WM.
Department of Neurology, Mayo Clinic, Rochester, MN, USA.
OBJECTIVE: To determine whether the time of onset of subarachnoid hemorrhage (SAH) or intracerebral hemorrhage (ICH) is associated with a time of day or season of year. BACKGROUND: Prior studies have suggested that there may be a circadian and seasonal pattern of ischemic stroke occurrence, but this is less certain for hemorrhagic stroke. Population-based data have been unavailable. METHODS: All incident ICH and SAH among residents of Rochester, MN, were ascertained. The medical records of patients were reviewed to determine the time of onset and date of occurrence. The day was divided into 8-hour periods, and the year into seasonal quartiles. Each patient was assigned a period based on the time of onset of symptoms. The data were analyzed by chi(2) analysis to determine whether there was a trend toward increased occurrence based on time period or seasonal quartile of onset. RESULTS: From 1960 to 1989, there were 155 cases (48 men, 107 women) of incident SAH. From 1975 to 1989, there were 137 cases (57 men, 80 women) of incident ICH. There was a significant increase in the time of onset for ICH and SAH in the 8 AM to 4 PM period (p = 0.005 and p = 0.03, respectively). The concomitant occurrence of hypertension, gender, and age did not affect the time of day of occurrence. In the analysis of seasonal variation, there was a significant increase in events during December, January, and February in the combined SAH and ICH group (p = 0.032) and a trend for SAH alone (p = 0.07) but not for ICH (p = 0.34). Hypertension and age had no impact on the association between season and the occurrence of SAH and ICH. CONCLUSION: The occurrence of SAH and ICH is increased from 8 AM to 4 PM. The occurrence of hemorrhage is increased during the winter months, but this is likely limited only to SAH.
Online source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11160954&dopt=Abstract hemorrhage
Exp Neurol. 2001 Feb;167(2):341-7.
Effect of FK-506 on inflammation and behavioral outcome following intracerebral hemorrhage in rat.
Peeling J, Yan HJ, Corbett D, Xue M, Del Bigio MR.
Department of Chemistry, The University of Manitoba, Winnipeg, Manitoba, R3E 0W3, Canada.
Beginning 15 min after induction of intracerebral hemorrhage (ICH) by intrastriatal administration of collagenase, rats were treated intramuscularly with FK-506 (3 mg/kg) or with vehicle. Treatment was repeated daily for 7 days. MR imaging 1, 7, and 28 days post-ICH showed that treatment did not affect hematoma size or its subsequent resolution. Two days post-ICH, neutrophil infiltration around the hematoma was decreased in the FK-506-treated rats, as was the number of TUNEL-positive cells at the edge of the hematoma and in the peripheral region. The decreased inflammatory response was accompanied by functional improvement in the treated rats. The neurological deficit induced by the ICH (beam walking ability, postural reflex, spontaneous circling) was significantly decreased from 3 to 21 days post-ICH by treatment with FK-506. Skilled use of the forelimb ipsilateral to the ICH was improved and sensory neglect of the same limb was decreased 8-9 weeks post-ICH in rats treated with FK-506. However, neuronal loss assessed 9 weeks post-ICH was not different in the treated and untreated rats. 2000 Academic Press.
Online source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11161622&dopt=Abstract hemorrhage
J Surg Res. 2001 Feb;95(2):126-32.
Assessment of topical hemostats in a renal hemorrhage model in heparinized rats.
Tuthill DD, Bayer V, Gallagher AM, Drohan WN, MacPhee MJ.
Holland Laboratory, American Red Cross, Rockville, Maryland, 20855, USA. tuthillsa.redcross.org
Various topical hemostatic agents or devices have been employed to address the challenges associated with hemorrhage from parenchymal organs during surgery or trauma. Their relative efficacy, however, has not been assessed in a single animal model. The objective of this study was to develop a small animal renal hemorrhage model for comparing hemostatic efficacy of various topical agents, and then to compare fibrin sealant (FS) to an existing standard of care for topical hemostasis. A left heminephrectomy was performed in anesthetized adult male Sprague-Dawley rats. Animals were anticoagulated with 2000 IU/kg heparin IV and various topical hemostatic agents were applied to the injury. Treatment groups included FS applied as a spray; FS applied through a cannula; gelatin sponge (GS) soaked in 1000 IU/mL thrombin solution; GS soaked in 300 IU/mL thrombin; dry GS; and fibrinogen without thrombin applied as a spray. The main endpoints of the study were incidence of hemostasis, blood loss, acute survival trends, and maintenance of mean arterial pressure (MAP). Three treatment groups, the two FS groups and the GS soaked in 1000 IU/mL thrombin, afforded significant hemostasis compared to the controls (P < 0.01). Both FS groups had significantly less blood loss, longer survival times, and maintained higher MAPs than the GS-treated groups. Quantitative dose effects and functional deficiencies in topical hemostatic products could be assessed using this animal model. The study demonstrated that liquid FS was significantly more efficacious than a GS soaked in thrombin for abating hemorrhage from a renal excision in a heparinized rat. 2000 Academic Press.
Online source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11162035&dopt=Abstract hemorrhage
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